Evidence mapPaperPMID 41280722Full record

ReviewResearch (Washington, D.C.)2025

Sepsis-Induced Endothelial Barrier Dysfunction: Mechanisms, Pathology, and Therapeutic Advances.

Rui Wang, Qiuju Han, Jiangbo Fan, Zhe Xu, Wenyi Liu, Di Liu, You Li, Juan Du, Jianhui Sun, Huacai Zhang and 5 more

Abstract readReview
In one paragraph

Review in Research (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 2 pooled it
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Rui WangState Key Laboratory of Trauma and Chemical Poisoning, Daping Hospital, Army Medical University, Chongqing 400042, China.ORCID https://orcid.org/0009-0001-6975-6872
Qiuju HanDepartment of Intensive Care Unit, Daping Hospital, State Key Laboratory of Trauma and Chemical Poisoning, Army Medical University, Chongqing 400042, China.
Jiangbo FanState Key Laboratory of Trauma and Chemical Poisoning, Daping Hospital, Army Medical University, Chongqing 400042, China.
Zhe XuDepartment of Emergency, the Affiliated Hospital of Guizhou Medical University, Guizhou Medical University, Guiyang 550001, China.
Wenyi LiuState Key Laboratory of Trauma and Chemical Poisoning, Daping Hospital, Army Medical University, Chongqing 400042, China.
Di LiuState Key Laboratory of Trauma and Chemical Poisoning, Daping Hospital, Army Medical University, Chongqing 400042, China.
You LiDepartment of Intensive Care Unit, Daping Hospital, State Key Laboratory of Trauma and Chemical Poisoning, Army Medical University, Chongqing 400042, China.
Juan DuState Key Laboratory of Trauma and Chemical Poisoning, Daping Hospital, Army Medical University, Chongqing 400042, China.
Jianhui SunState Key Laboratory of Trauma and Chemical Poisoning, Daping Hospital, Army Medical University, Chongqing 400042, China.
Huacai ZhangState Key Laboratory of Trauma and Chemical Poisoning, Daping Hospital, Army Medical University, Chongqing 400042, China.
Qingli CaiState Key Laboratory of Trauma and Chemical Poisoning, Daping Hospital, Army Medical University, Chongqing 400042, China.
Chu GaoState Key Laboratory of Trauma and Chemical Poisoning, Daping Hospital, Army Medical University, Chongqing 400042, China.
Jianxin JiangState Key Laboratory of Trauma and Chemical Poisoning, Daping Hospital, Army Medical University, Chongqing 400042, China.
Zhen WangDepartment of Intensive Care Unit, Daping Hospital, State Key Laboratory of Trauma and Chemical Poisoning, Army Medical University, Chongqing 400042, China.
Ling ZengState Key Laboratory of Trauma and Chemical Poisoning, Daping Hospital, Army Medical University, Chongqing 400042, China.ORCID https://orcid.org/0000-0002-9640-9083

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is a life-threatening disease characterized by systemic inflammation and endothelial barrier dysfunction, leading to multiorgan failure and high mortality. This review provides a comprehensive overview of the pathological mechanisms underlying sepsis-induced endothelial dysfunction, focusing on glycocalyx degradation, endothelial cell death, increased vascular permeability, and coagulopathy. During sepsis, the endothelial glycocalyx (EG) is disrupted, leading to increased vascular permeability and impaired microcirculation. Endothelial cells undergo various forms of cell death, including apoptosis, pyroptosis, ferroptosis, and autophagy, which are driven by inflammation and oxidative stress. These processes are further complicated by the activation of coagulation pathways and the formation of intravascular thrombi. The interaction between endothelial cells and immune cells amplifies the inflammatory response, contributing to the persistence of systemic inflammation. We also discuss emerging therapeutic strategies aimed at protecting endothelial cells, modulating inflammation, and improving coagulation function, including glycocalyx protectants, anti-inflammatory agents, anticoagulants, and endothelial repair mechanisms. Future research should focus on translating these therapeutic approaches into clinical practice to improve outcomes in patients with sepsis.

Identifiers

PMID41280722
PMCPMC12635411

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.